The majority of the cancer therapeutics act in a relatively nonspecific fashion to kill rapidly dividing cancer cells, often through DNA damage that can lead to significant toxicities or other complications. Recently, drugs that target specific protein-protein or protein-RNA interactions became more attractive as they offer several advantages with regard to efficacy and toxicity. In normal cellular physiology, p53 functions as a tumor suppressor protein that plays a central role in controlling cell cycle progression and apoptosis. Due to this critical role, p53 is considered as an attractive cancer therapeutic target because stimulating its tumor suppressor activity can potentially eradicate tumor cell growth. The present invention presents a novel class of chemicals that targets the protein called HDMX. HDMX physiologically plays major role in survival of cancer cells. In normal cellular conditions, p53 is negatively regulated by both HDMX and HDM2 proteins. It has been demonstrated that Nutlin-3 induced inhibition of HDM2 causes cell death by inducing p53, independent of DNA damage. A variant of Nutlin-3 is currently undergoing clinical trials; however, use of these analogs is limited as they do not affect HDMX which suppresses p53 in a much large subset of cancer cells than HDM2. HDMX, a structural homolog of HDM2, can be successfully targeted by the compounds of the present invention and induce cell cycle arrest and subsequently cause apoptotic cell death. In the present invention, the structures and synthesis of these compounds are presented as well as analysis of activity in disrupting p53-HDMX interactions that are based on the acridine scaffold.